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Showing 1–8 of 8 results
Advanced filters: Author: Lora M. Jensen Clear advanced filters
  • Combining ancestral protein reconstruction with deep mutational scanning to characterize alternative histories in the sequence space around an ancient transcription factor reveals hundreds of alternative protein sequences that use diverse biochemical mechanisms to perform the derived function at least as well as the historical outcome.

    • Tyler N. Starr
    • Lora K. Picton
    • Joseph W. Thornton
    Research
    Nature
    Volume: 549, P: 409-413
  • The Cancer Genome Atlas Research Network reports an integrative analysis of more than 400 samples of clear cell renal cell carcinoma based on genomic, DNA methylation, RNA and proteomic characterisation; frequent mutations were identified in the PI(3)K/AKT pathway, suggesting this pathway might be a potential therapeutic target, among the findings is also a demonstration of metabolic remodelling which correlates with tumour stage and severity.

    • Chad J. Creighton
    • Margaret Morgan
    • Heidi J. Sofia.
    ResearchOpen Access
    Nature
    Volume: 499, P: 43-49
  • The Cancer Genome Atlas consortium reports on their genome-wide characterization of somatic alterations in colorectal cancer; in addition to revealing a remarkably consistent pattern of genomic alteration, with 24 genes being significantly mutated, the study identifies new targets for therapeutic intervention and suggests an important role for MYC-directed transcriptional activation and repression.

    • Donna M. Muzny
    • Matthew N. Bainbridge
    • Elizabeth Thomson.
    ResearchOpen Access
    Nature
    Volume: 487, P: 330-337
  • Current clinical practice is organized according to tissue or organ of origin of tumors. Now, The Cancer Genome Atlas (TCGA) Research Network has started to identify genomic and other molecular commonalities among a dozen different types of cancer. Emerging similarities and contrasts will form the basis for targeted therapies of the future and for repurposing existing therapies by molecular rather than histological similarities of the diseases.

    • Kyle Chang
    • Chad J Creighton
    • Joshua M Stuart
    Comments & OpinionOpen Access
    Nature Genetics
    Volume: 45, P: 1113-1120